Objective To investigate the change and role of nitric oxide (NO), nitric oxide synthase (NOS) in serum of children with Epilepsy.Methods The serum NO and NOS levels of 58 epileptic children and 23 healthy children were measured with enzyme linked immunosorbent assay (ELISA). Results The concentrations of the serum NO [( 5.86? 1.21)?mol/ml] and NOS [( 28.26? 8.49)U/ml] in patient group were significantly higher than those in control group [( 3.78? 0.74)?mol/ml,( 17.86? 4.58)U/ml)]( P

Objective To evaluated the improving effect of training method of point-line-plane on development quotient in premature infants with brain injury.Methods 174 cases of premature children with brain injury were randomly divided into study group (89 cases) and control group (85 cases).Control group given Bobath and Vojta traditional rehabilitation training,and the study group was given training method of point-line-plane.Patients in both groups were evaluated synthetically based on The Evaluation Chart on Neu-robehavioral Development of Children Aged 0-6 Years,developed by Capital Institute of Pediatrics,prior to the treatment,and after the first,the second,and the third course of the training programs,respectively.Re-sults The score of developmental quotient ( DQ) between study group and control group was no significantly different(P>0.05).Compared with before treatment, the scores of DQ was significantly increased after the first, the second and the third course of training treatment in study group and control group((82.71±12.28) vs (81.17±9.63), t=0.859, P>0.05;(89.65±10.02) vs (87.02±7.39), t=1.747, P>0.05). Compared with the control group, the scores of DQ in study group was no significant difference after the first and the second course of treatment,but there was significantiy different after the third course treatment((95.26±8.87) vs (91.31±7.63), t=2.945, P=0.004).Conclusion The training method of point-line-plane can improve the clinical efficacy of premature infants with brain injury at the early phase, which is worth widely applying in clinical practice.

Traumatic brain injury (TBI)-induced coagulopathy has increasingly been recognized as a significant risk factor for poor outcomes, but the pathogenesis remains poorly understood. In this study, we aimed to investigate the causal role of acrolein, a typical lipid peroxidation product, in TBI-induced coagulopathy, and further explore the underlying molecular mechanisms. We found that the level of plasma acrolein in TBI patients suffering from coagulopathy was higher than that in those without coagulopathy. Using a controlled cortical impact mouse model, we demonstrated that the acrolein scavenger phenelzine prevented TBI-induced coagulopathy and recombinant ADAMTS-13 prevented acrolein-induced coagulopathy by cleaving von Willebrand factor (VWF). Our results showed that acrolein may contribute to an early hypercoagulable state after TBI by regulating VWF secretion. mRNA sequencing (mRNA-seq) and transcriptome analysis indicated that acrolein over-activated autophagy, and subsequent experiments revealed that acrolein activated autophagy partly by regulating the Akt/mTOR pathway. In addition, we demonstrated that acrolein was produced in the perilesional cortex, affected endothelial cell integrity, and disrupted the blood-brain barrier. In conclusion, in this study we uncovered a novel pro-coagulant effect of acrolein that may contribute to TBI-induced coagulopathy and vascular leakage, providing an alternative therapeutic target.